g0/g1 phase

Ailanthone (AIL) is a natural compound derived from the tree Ailanthus altissima and has anti-hepatocellular carcinoma (HCC) properties. It can induce G0 G1 phase cell cycle arrest by downregulating the expression of cyclins and CDKs, while upregulating the expression of p21 and p27. Additionally, Ailanthone is a potent androgen receptor (AR) inhibitor, capable of inhibiting both the full-length androgen receptor (IC50: 69 nM) and constitutively active splice variants (IC50: 309 nM).

Meisoindigo (Natura-α) is a derivative of indigo natural, might induces apoptosis and myeloid differentiation of acute myeloid leukemia (AML).

Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013). Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3 References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013).

9-hydroxy Stearic Acid is a hydroxy fatty acid that is the active metabolite of 9-PAHSA. 9-hydroxy Stearic Acid is formed from 9-PAHSA through carboxyl ester lipase in the liver and pancreas. The 9-hydroxy Stearic Acid (5 μM) was stearic acid, which inhibited the expression of histone deacetylase 1 (HDAC1) in the lysate of HT-29 colon cancer cells. 3. When the concentration was 100 μM.1, the proliferation of HT-29 cells was inhibited and cell cycle arrest was induced in G0 g1 phase.

Prim-O-glucosylcimifugin (Cimifugin 7-glucoside) can inhibit the proliferation of SMC(smooth muscle cell) stimulated by TNF-alpha, increase the proportion of G0 G1 phase.

Asparanin A, an apoptosis inducer with anticancer properties, arrests the cell cycle in the G0 G1 phase via the mitochondria and PI3K AKT signaling pathways. It effectively inhibits cancer cell proliferation and has shown in vivo efficacy in a mouse xenograft model of Ishikawa endometrial carcinoma, significantly reducing tumor growth [1].

Capillarisin is a novel blocker of STAT3 activation and thus may have a potential in negative regulation of growth, metastasis, and chemoresistance of tumor cells, it inhibits cancer cell growth of osteosarcoma cells by inducing apoptosis accompanied with

Bostrycin, an anthraquinone derived from B. alpestre, exhibits a broad spectrum of biological activities including antibacterial, antiproliferative, and phytotoxic effects. This compound demonstrates efficacy against Gram-positive bacteria like methicillin-resistant S. aureus (MRSA), M. tuberculosis, and C. botulinum. Additionally, Bostrycin shows antiproliferative action against A549 lung adenocarcinoma cells, particularly by arresting the cell cycle at the G0/G1 phase and triggering apoptosis within a concentration range of 10 to 30 µM. As a phytotoxin, it causes necrosis in water hyacinth leaves at approximately 7 µg/ml. Furthermore, Bostrycin serves as a protein immobilization cross-linking agent, managing to preserve its bacteriostatic properties when affixed to nonwoven polypropylene fabric.

PI3K AKT-IN-4 (compound 3), a diterpenoid extracted from the roots and rhizomes of Salvia castanea Dielsf., exhibits antitumor properties by inhibiting cell viability and proliferation (IC 50 =4.72 μM) and promoting apoptosis in Hep3B cells. This compound obstructs the G0 G1 phase of the cell cycle, triggers mitochondrial dysfunction, and induces oxidative stress. Moreover, PI3K AKT-IN-4 combats hepatocellular carcinoma through the inhibition of the PI3K-Akt signaling pathway and by interacting with PARP1 and CDK2 targets.

Aphidicolins B32 is a diterpene compound identified in the marine fungus Botryotinia fuckeliana. It exhibits cytotoxic activity against human bladder cancer cells by inhibiting the proliferation of T24 cells at the G0 G1 phase, with an IC50 of 27.6 μM. Aphidicolins B32 is applicable for research in the field of anticancer studies.